Achalasia is a motility disorder of the esophagus wherein a frequently hypertensive lower esophageal sphincter (LES) fails to completely relax accompanied with a lack of peristalsis in the tubular esophagus. The major symptom of patients suffering from achalasia is difficulty swallowing (dysphagia). Other common symptoms include stagnation of swallowed solids and liquids (stasis), regurgitation, weight loss, chest pain, nocturnal cough, and secondary respiratory complications. Although the exact cause of achalasia is unknown, recent studies have suggested that achalasia is an autoimmune disease triggered by some insult, perhaps a virus, in individuals genetically susceptible to the disease. Left untreated, achalasia can worsen and complications include pulmonary disease secondary to chronic aspiration, megaesophagus, and cancer.
Individuals exhibiting symptoms of achalasia are often diagnosed through imaging studies (ultrasound and barium esophagogram), manometry, esophagogastroduodenoscopy (EGD), manometry, and high resolution manometry (HRM) with pressure topography plotting. Elevated LES pressure on manometry, aperistalsis of the smooth muscle of the esophagus, and incomplete relaxation of the LES are the most common features of classic achalasia. Achalasia is considered the antithesis of gastroesophageal reflux disease (GERD), as patients suffering from achalasia exhibit elevated LES pressures and increased LES tone while those with GERD have decreased LES pressures and decreased LES tone. However, patients with achalasia do sometimes experience reflux symptoms, possibly due to retention of acidic food contents or bacterial overgrowth with resultant lactate production in the esophagus.
Since an exact cause is not known, current treatment modalities for achalasia are targeted at relieving symptoms. These treatments include pharmacologic therapy, endoscopy, and surgery. Pharmacologic therapies act to treat achalasia by reducing LES pressure through the use of smooth muscle relaxants. Common medications include calcium channel blockers, nitrates, and phosphodiesterase 5 inhibitors. These are taken shortly before meals and provide limited LES relaxation. Unfortunately, patients still often complain of dysphagia despite relaxation of the LES. In addition, pharmacologic agents have a short duration of action and their use is associated with a large number of side effects. As such, pharmacologic therapy is mostly intended for patients with a new onset of achalasia or for those who are awaiting more long term treatment.
Endoscopic therapies available in the treatment of achalasia include pneumatic dilation of the LES and botulinum toxin injection into the LES. Pneumatic dilation involves passing an inflatable balloon into the patient's mouth and advancing it to the LES, at which point the balloon is inflated with the desired result being disruption of the LES. Pneumatic dilation has been considered the most effective non-surgical treatment of achalasia. However, pneumatic dilation runs the risk of esophageal perforation and studies show symptoms of achalasia return in approximately 50% of patients after 15 years.
Botulinum toxin injection involves injecting a small amount of botulinum toxin into the area of the LES of the affected patient. The neurotoxin blocks the release of acetylcholine from excitatory neurons, resulting in relaxation of the LES. For example, U.S. Pat. No. 5,437,291, assigned to Allergan, Inc., describes a “method for in vivo treatment of smooth muscle disorders of a mammal, comprising: injecting directly into a smooth muscle in a mammal an amount of a neurotoxin which inhibits neurotransmitter release from nerve terminals.” In addition, U.S. Pat. No. 8,025,889, assigned to Patricia S. Walker, describes a “method for treating a condition in a patient in need thereof, the method comprising the step of locally administering a therapeutically effective amount of a botulinum toxin in powder form to the patient using a needleless injector, wherein the condition is selected from the group consisting of spasmodic dysphonia, laryngeal dystonia, oromandibular dysphonia, lingual dystonia, cervical dystonia, focal hand dystonia, blepharospasm, strabismus, hemifacial spasm, eyelid disorder, cerebral palsy, focal spasticity, spasmodic colitis, neurogenic bladder, anismus, limb spasticity, tics, tremors, bruxism, anal fissure, achalasia, fibromyalgia, dysphagia, lacrimation, hyperhydrosis, excessive salivation, excessive gastrointestinal secretions, excessive mucous secretion, pain from muscle spasms, headache pain, brow furrows and skin wrinkles, whereby a symptom of the condition is thereby alleviated within 1 to 7 days.”
Although botulinum toxin injections have been shown to be safe, 50% of patients have recurrence of symptoms after one year and nearly all patients have recurrence of symptoms after two years. Therefore, repeated treatments are often necessary to treat symptoms.
Surgical options for treating achalasia include myotomy and subtotal esophageal resection. Perforation is a risk associated with LES myotomy, and, although prognosis is quite good following the treatment, many patients suffer from severe GERD post-surgery. Therefore, a fundoplication is included with most myotomy procedures. A laparoscopic Heller myotomy with some type of fundoplication has become the preferred and most effective surgical therapy. However, some patients continue to experience GERD and require additional anti-reflux therapies. Subtotal esophageal resection with gastric pull-up is typically reserved for patients who do not respond to any other treatment. While effective, this procedure is extremely invasive and is associated with a high post-operative morbidity.
Therefore, a need exists for a safe, minimally invasive therapy for achalasia with high long-term efficacy. What is also needed is a treatment for achalasia that is not associated with the numerous side effects encountered with prior art therapies.
Hiatal hernia formation and recurrence is commonly encountered in patients suffering from gastroesophageal reflux disease (GERD). A hiatal hernia is a protrusion of a portion of the stomach through the diaphragm and up into the thorax. Patients having a hiatal hernia experience discomfort associated with reflux of stomach contents as the hiatal hernia impairs the function of the lower esophageal sphincter. Therefore, there is a need for a device and a method for treating GERD that would also prevent the formation or recurrence of a hiatal hernia.
Esophageal foreshortening is an occurrence seen in patients with GERD in which the length of the esophagus shortens and the gastroesophageal junction (GEJ) is briefly pulled upward into the thorax. In a manner similar to that seen with a hiatal hernia, esophageal foreshortening impairs the function of the LES by interfering with its complete closure. This results in decreased competency of the gastroesophageal barrier and leads to GERD. Esophageal foreshortening is also believed to be partly responsible for transient LES relaxations (TLESRs). TLESRs are brief episodes of reflux caused by the loss of LES tone. Esophageal shortening can cause migration of the GEJ into the thorax and, when immediately followed by relaxation of the LES, can result in the reflux of stomach contents back into the esophagus. Therefore, there is a need for a device and a method for treating GERD that would also prevent esophageal foreshortening.